Bartzokis G, Sultzer D, Cummings J, Holt L E, Hance D B, Henderson V W, Mintz J
Department of Psychiatry, University of Arkansas for Medical Sciences and the Mental Health Service, Central Arkansas Veterans Healthcare System, Little Rock, USA.
Arch Gen Psychiatry. 2000 Jan;57(1):47-53. doi: 10.1001/archpsyc.57.1.47.
The basal ganglia contain the highest levels of iron in the brain, and postmortem studies indicate a disruption of iron metabolism in the basal ganglia of patients with Alzheimer disease (AD). Iron can catalyze free radical reactions and may contribute to oxidative damage observed in AD brains. Treatments aimed at reducing oxidative damage have offered novel ways to delay the rate of progression and could possibly defer the onset of AD. Brain iron levels were quantified in vivo using a new magnetic resonance imaging method.
Thirty-one patients with AD and 68 control subjects participated in this study. A magnetic resonance imaging method was employed that quantifies the iron content of ferritin molecules (ferritin iron) with specificity through the combined use of high and low field-strength magnetic resonance imaging instruments. Three basal ganglia structures (caudate, putamen, and globus pallidus) and one comparison region (frontal lobe white matter) were evaluated.
Basal ganglia ferritin iron levels were significantly increased in the caudate (P = .007; effect size, 0.69) and putamen (P = .008; effect size, 0.67) of AD subjects, with a trend toward an increase in the globus pallidus (P = .13). The increased basal ganglia ferritin iron levels were not a generalized phenomenon; white matter ferritin iron levels were unchanged in patients with AD (P = .50).
The data replicate and extend prior results and suggest that basal ganglia ferritin iron levels are increased in AD. Prospective studies are needed to evaluate whether premorbid iron levels are increased in individuals who develop AD.
基底神经节是大脑中铁含量最高的部位,尸检研究表明,阿尔茨海默病(AD)患者基底神经节的铁代谢存在紊乱。铁可催化自由基反应,并可能导致AD大脑中观察到的氧化损伤。旨在减少氧化损伤的治疗方法提供了延缓疾病进展速度的新途径,并可能推迟AD的发病。采用一种新的磁共振成像方法对脑铁水平进行体内定量。
31例AD患者和68例对照者参与了本研究。采用一种磁共振成像方法,通过联合使用高场强和低场强磁共振成像仪器,特异性地定量铁蛋白分子中的铁含量(铁蛋白铁)。评估了三个基底神经节结构(尾状核、壳核和苍白球)和一个对照区域(额叶白质)。
AD患者尾状核(P = .007;效应量,0.69)和壳核(P = .008;效应量,0.67)的基底神经节铁蛋白铁水平显著升高,苍白球有升高趋势(P = .13)。基底神经节铁蛋白铁水平升高并非普遍现象;AD患者白质铁蛋白铁水平无变化(P = .50)。
这些数据重复并扩展了先前的结果,表明AD患者基底神经节铁蛋白铁水平升高。需要进行前瞻性研究,以评估患AD个体的病前铁水平是否升高。